The term HTLV (human T-cell leukemia/lymphoma virus) denotes an extended family of retroviruses. There are currently three known members of this family (HTLV-I, HTLV-II, and HTLV-III), and it is quite likely that more members will be discovered in the future. This first two members have been linked to human neoplasms, and HTLV-I (the virus about which the most is known) has been linked to the pathogenesis of adult T-cell leukemia. The most recently discovered member of the HTLV family (HTLV-III) is thought to be the etiologic agent of acquired immunodeficiency syndrome (AIDS), and it has several immunologic and biochemical features in common with the other viruses. Very little is known about how infection and integration of HTLV into the genome will affect the immune function of T cells that themselves have reactivity for the virus. The purpose of the current project was to characterize the functional consequences of HTLV-infection in HTLV-specific T cells using the first member of the family (HTLV-I) as a prototype. The results indicate that HTLV-I can transform clones with a helper/inducer phenotype as well as clones with a suppressor/cytotoxic phenotype. This transformation can be associated with a progressive loss of T-cell function or a cytopathic effect on the target cell under the appropriate circumstances.